Evidence map›Paper›PMID 15231802›Full record

ArticleJournal of bacteriology2004

Delineation of upstream signaling events in the salmonella pathogenicity island 2 transcriptional activation pathway.

Charles C Kim, Stanley Falkow

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. mBio · 2023
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Frontiers in microbiology · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Charles C KimMicrobiology and Immunology, 299 Campus Drive, Stanford University Medical Center, Stanford, CA 94305, USA. cckim@stanford.edu
Stanley Falkow
Stanford Medicine · USStanford University · US

Funding

GENETIC AND MOLECULAR BASIS OF BACTERIAL INVASTIONR01AI026195 · NIAID · STANFORD UNIVERSITY · PI FALKOW, STANLEY · 1988 to 2007
$2.8M
NIAID NIH HHS AI26195NIAID NIH HHS R01 AI026195
6 · The paper itself

Abstract

Survival and replication in the intracellular environment are critical components of the ability of Salmonella enterica serovar Typhimurium to establish systemic infection in the murine host. Intracellular survival is mediated by a number of genetic loci, including Salmonella pathogenicity island 2 (SPI2). SPI2 is a 40-kb locus encoding a type III secretion system that secretes effector molecules, which permits bacterial survival and replication in the intracellular environment of host cells. A two-component regulatory system, ssrAB, is also encoded in SPI2 and controls expression of the secretion system and effectors. While the environmental signals to which SPI2 responds in vivo are not known, activation of expression is dependent on OmpR and can be stimulated in vitro by chelation of cations or by a shift from rich to acidic minimal medium. In this work, we demonstrated that SPI2 activation is associated with OmpR in the phosphorylated form (OmpR-P). Mutations in envZ and ackA-pta, which disrupted two distinct sources of OmpR phosphorylation, indicated that SPI2 activation by chelators or a shift from rich to acidic minimal medium is largely dependent on functional EnvZ. In contrast, the PhoPQ pathway is not required for SPI2 activation in the presence of OmpR-P. As in the case of in vitro stimulation, SPI2 expression in macrophages correlates with the presence of OmpR-P. Additionally, EnvZ, but not acetyl phosphate, is required for maximal expression of SPI2 in the intracellular environment, suggesting that the in vitro SPI2 activation pathway is the same as that used in vivo.

Indexed as

Escherichia coli ProteinsGene Expression Regulation, BacterialSignal TransductionTranscriptional ActivationAcetate KinaseAnimalsBacterial Outer Membrane ProteinsBacterial ProteinsCell LineChelating AgentsGene DeletionGenomic IslandsHydrogen-Ion ConcentrationMacrophagesMembrane ProteinsMiceAcetate KinaseBacterial Outer Membrane ProteinsBacterial ProteinsChelating AgentsenvZ protein, E coliEscherichia coli ProteinsMembrane ProteinsMultienzyme Complexesosmolarity response regulator proteinsPhoP protein, BacteriaPhoQ protein, BacteriaPhosphate AcetyltransferaseRNA, BacterialSPI-2 protein, SalmonellaSsrB protein, Salmonella typhimuriumtmRNATrans-ActivatorsTranscription Factors

Identifiers

PMID15231802
PMCPMC438577
OpenAlexW2101695227

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.